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首页> 外文期刊>Cell biology international. >The effect of vaccination with the lysate of heat-shocked tumor cells on nitric oxide production in BALB/c mice with fibrosarcoma tumor.
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The effect of vaccination with the lysate of heat-shocked tumor cells on nitric oxide production in BALB/c mice with fibrosarcoma tumor.

机译：用热休克的肿瘤细胞裂解液接种疫苗对纤维肉瘤肿瘤BALB / c小鼠中一氧化氮产生的影响。

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摘要

The aim of this study was to investigate the effect of heat shock protein-70 (HSP-70) on splenocyte proliferation and nitric oxide (NO) production in the BALB/c mice fibrosarcoma tumor model. To do so, HSP-70 was induced in the lysate of heat-shocked tumor cells and WEHI-164 cells (mouse fibrosarcoma cell line) were injected subcutaneously into the right flank of inbred BALB/c mice to establish a tumor model. Three animal bearing tumor groups were applied: the test group; vaccinated with HSP-70 enriched tumor lysate; control group I, vaccinated with tumor lysate only; and control group II, which received PBS. Using immunoblot analysis, an increase of HSP-70 expression was detected in the lysate of heat-shocked cells in comparison with non-heat-shocked cells. The effect of the test lysate on NO production was measured both in vitro and in vivo in the peritoneal macrophages and splenocytes of tumor bearing mice, respectively. The result showed a significant increase in NO production both in vitro by peritoneal macrophages and in vivo after immunization with HSP-70 enriched tumor lysate. In addition, tumor growth was significantly postponed and the proliferation of splenocytes was increased in the test group. Our results indicate that the lysate of heat-shocked tumor cells was more potent than that of non-heat-shocked tumor cells in inducing anti-tumor immunity. Since production of NO by HSP-activated antigen presenting cells (APCs) is likely to affect innate immunity and tumor growth, the probable mechanism of postponing tumor growth would be NO production by innate immune cells. These findings provide a useful therapeutic model for developing novel approaches to cancer treatments.
机译：这项研究的目的是研究热休克蛋白70（HSP 70）对BALB / c小鼠纤维肉瘤肿瘤模型中脾细胞增殖和一氧化氮（NO）产生的影响。为此，在热休克的肿瘤细胞的裂解物中诱导HSP-70，并将WEHI-164细胞（小鼠纤维肉瘤细胞系）皮下注射到近交BALB / c小鼠的右胁腹以建立肿瘤模型。应用了三个带有动物肿瘤的组：试验组;动物组。接种了富含HSP-70的肿瘤裂解液;对照组I，仅接种肿瘤溶解物;对照组PBS。使用免疫印迹分析，与非热激细胞相比，在热激细胞的裂解物中检测到HSP-70表达的增加。在体外和体内分别在荷瘤小鼠的腹膜巨噬细胞和脾细胞中测量了测试裂解物对NO产生的影响。结果表明，在体外通过腹膜巨噬细胞和在用富含HSP-70的肿瘤裂解液免疫后体内，NO产量均显着增加。另外，在测试组中，肿瘤的生长被显着推迟并且脾细胞的增殖增加。我们的结果表明，热激肿瘤细胞的裂解物在诱导抗肿瘤免疫方面比非热激肿瘤细胞更有效。由于由HSP激活的抗原呈递细胞（APC）产生NO可能会影响先天免疫和肿瘤生长，因此推迟肿瘤生长的可能机制可能是先天免疫细胞产生NO。这些发现为开发新的癌症治疗方法提供了有用的治疗模型。

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